E-C coupling failure in mouse EDL muscle after in vivo eccentric contractions

E-C coupling failure in mouse EDL muscle after in vivo eccentric contractions Abstract The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (P o ) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice ( n = 164) were injured in vivo with 150 eccentric contractions. P o , caffeine-, 4-chloro- m -cresol-, and K + -induced contracture forces, sarcoplasmic reticulum (SR) Ca 2+ release and uptake rates, and intracellular Ca 2+ concentration (Ca 2+ i ) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in P o (∼51%) compared with caffeine-induced force (∼11–21%), we estimate that E-C coupling failure can explain 57–75% of the P o decrement from 0 to 5 days postinjury. Comparable reductions in P o and K + -induced force (51%), and minor reductions (0–6%) in the maximal SR Ca 2+ release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting Ca 2+ i was elevated and peak tetanic Ca 2+ i was reduced, whereas peak 4-chloro- m -cresol-induced Ca 2+ i was unchanged immediately after injury. By 3 days postinjury, 4-chloro- m -cresol-induced Ca 2+ i became depressed, probably because of decreased SR Ca 2+ release and uptake rates (17–31%). These data indicate that the decrease in P o during the first several days after injury primarily stems from a failure in the E-C coupling process. excitation-contraction extensor digitorum longus fluo 3 fura red calcium-selective minielectrode Footnotes Address for reprint requests: C. P. Ingalls, Muscle Biology Laboratory, Dept. of Health and Kinesiology, Texas A&M Univ., College Station, TX 77843-4243 (E-mail: Ingalls@unix.tamu.edu ). Copyright © 1998 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

E-C coupling failure in mouse EDL muscle after in vivo eccentric contractions

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
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Abstract

Abstract The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (P o ) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice ( n = 164) were injured in vivo with 150 eccentric contractions. P o , caffeine-, 4-chloro- m -cresol-, and K + -induced contracture forces, sarcoplasmic reticulum (SR) Ca 2+ release and uptake rates, and intracellular Ca 2+ concentration (Ca 2+ i ) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in P o (∼51%) compared with caffeine-induced force (∼11–21%), we estimate that E-C coupling failure can explain 57–75% of the P o decrement from 0 to 5 days postinjury. Comparable reductions in P o and K + -induced force (51%), and minor reductions (0–6%) in the maximal SR Ca 2+ release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting Ca 2+ i was elevated and peak tetanic Ca 2+ i was reduced, whereas peak 4-chloro- m -cresol-induced Ca 2+ i was unchanged immediately after injury. By 3 days postinjury, 4-chloro- m -cresol-induced Ca 2+ i became depressed, probably because of decreased SR Ca 2+ release and uptake rates (17–31%). These data indicate that the decrease in P o during the first several days after injury primarily stems from a failure in the E-C coupling process. excitation-contraction extensor digitorum longus fluo 3 fura red calcium-selective minielectrode Footnotes Address for reprint requests: C. P. Ingalls, Muscle Biology Laboratory, Dept. of Health and Kinesiology, Texas A&M Univ., College Station, TX 77843-4243 (E-mail: Ingalls@unix.tamu.edu ). Copyright © 1998 the American Physiological Society

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Jul 1, 1998

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